The neuro-endocrine model has reached a wide consensus as one of the basic mechanisms for progressive heart failure based on the good results obtained by ACE-inhibitor therapy . A decade ago the cytokine model was added to explain the syndrome of heart failure . The cytokines are highly potent endogenous peptides produced by different cell types . Elevated levels might be markers for cardiac cachexia, but they may also play an important role in the mechanism of CHF progression . Subsequently, the muscle hypothesis was proposed as an explanation for the deconditioning in CHF patients . In skeletal muscle from healthy individuals there is a balanced distribution between type I fibres (aerobic), type IIA fibres (both aerobic and anaerobic) and type IIB fibres (mostly anaerobic). In CHF a shift to type II fibres and a reduced capillary density as well as a reduced cytochrome oxidase activity is observed, but the mechanisms leading to such a shift have not been clarified . Deconditioning may be an important factor aggravating the underlying pathophysiology in CHF and exercise training has been shown to improve exercise performance and to reduce symptoms in this population . This is partly mediated by activation of the Protein PGC-1, a critical factor coordinating the activation of metabolic genes required for substrate utilization and mitochondrial biogenesis . The increase in this enzyme has been highly correlated to increase in peak VO2 after a aerobic interval training program in heart failure .